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260 Catheter-directed thrombolysis, mechanical thrombectomy, and surgery
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Iliofemoral venous thrombectomy is then performed by
passing a No. 8 or 10 venous thrombectomy balloon catheter partially into the iliac vein for several passes to remove
the bulk of the thrombus before advancing the catheter into
the vena cava. e proximal thrombectomy is always performed under uoroscopic guidance, with contrast material in the balloon, especially if a vena caval lter is present,
there is clot in the vena cava, or resistance to catheter passage is encountered. During this part of the procedure, the
anesthesiologist applies positive end-expiratory pressure
to further reduce the risk of pulmonary embolization. If
a clot is present in the vena cava, caval thrombectomy can
be performed with a protective balloon catheter inated
above thethrombus as an alternative to vena caval ltration
(Figure 20.5g).
Aer completion of the iliofemoral venous thrombectomy, intraoperative phlebography/uoroscopy is performed to evaluate for an underlying iliac vein stenosis and
to assess the nature of the venous drainage into the vena
cava. Intravascular ultrasound is better than single-view
phlebography for detecting iliac vein stenosis. Any underlying iliac vein stenosis is corrected by balloon angioplasty
and stenting if venous recoil occurs. If an iliac vein stent is
used, a 14-mm diameter or larger stent is recommended for
the common iliac vein and 12-mm diameter or larger stent
for the external iliac vein.
Once the venotomy is closed, an end-to-side arteriovenous stula (AVF) is constructed by anastomosing the
amputated end of the proximal saphenous vein or a large
proximal branch of the saphenous vein to the side of the
supercial femoral artery. e anastomosis should be limited to 3.5–4.0 mm in diameter. e purpose of the AVF is to
increase venous velocity but not venous pressure. Common
femoral vein pressure is recorded before and aer the
AVF is opened. No increase in venous pressure should be
observed when the AVF is opened. If the pressure increases,
the proximal iliac vein should be re-evaluated for residual
stenosis or obstruction and the proximal lesion corrected.
If the pressure remains elevated, the AVF is constricted to
decrease ow and normalize pressure.
A piece of polytetrauoroethylene or bovine pericardium
is wrapped around the saphenous AVF and a large permanent monolament suture (No. 0) looped and clipped with
approximately 2 cm le in the subcutaneous tissue (Figure
20.5h). is will serve as a guide for future dissection in the
event that operative closure of the AVF becomes necessary,
although most, if not all, AVFs do not require closure. Since
the AVF is limited and cannot enlarge, we consider it permanent. Clinical experience has shown a re-thrombosis rate
of 12%–18% following elective closure of AVFs. ese AVFs
may also be closed with obliteration of the stula using an
endovascular intervention.
If serous wound accumulation is observed, a diligent
search for transected lymphatics is performed, with careful
ligation and coagulation. A closed suction drain is generally
placed in the wound to evacuate serosanguineous uid that
may accumulate post-operatively. e drain exits through a
separate puncture site adjacent to the incision. e wound
is closed with multilayered running absorbable sutures to
achieve hemostatic and lymphostatic wound closure and
ensure elimination of dead space.
e distal posterior tibial vein is ligated. A small infusion catheter (pediatric feeding tube) is brought into the
wound via a separate stab incision in the skin and inserted
and xed in the proximal posterior tibial vein (Figure 20.5i).
is catheter is used for post-operative anticoagulation with
unfractionated heparin (UFH) and pre-discharge phlebography. Anticoagulation via this catheter ensures maximum
heparin concentration in the aected veins during their
period of greatest thrombogenicity. A 2–0 monolament
suture is looped around the proximal posterior tibial vein
(and catheter) and both ends exit the skin adjacent to the
wound. e ends of the suture are passed through the holes
of a sterile button, which is secured snugly to the skin when
the catheter is removed. Upward tension on the ends of the
suture obliterates the proximal posterior tibial vein at the
time of catheter removal and eliminates the risk of bleeding;
the suture is tied and secured above the skin by the button.
As mentioned, before removal of the catheter, an ascending phlebogram is performed through the catheter to assess
phlebographic patency.
Antibiotic ointment is applied to all wounds beneath
sterile dressings. e patient’s leg is wrapped snugly with
sterile gauze and multilayered elastic bandages from the
base of the toes to the groin. e posterior tibial vein catheter exits between the layers of the bandage, but is secured
so that the patient can ambulate using an intravenous pole
on wheels to support infusion of UFH.
20.8 POST-OPERATIVE CARE
erapeutic anticoa gulation is continued wit h UFH through
the posterior tibial vein catheter attached to a pump on an
intravenous pole with wheels so that the patient can ambulate. Before removal of the posterior tibial vein catheter, an
ascending phlebogram is performed. Oral anticoagulation
is begun when the patient awakens and resumes oral intake.
Heparin infusion is continued for an overlap of 4–5 days
until the international normalized ratio reaches 2–3. Oral
anticoagulation is continued for an extended period, generally for a period of 1 year or more.
Intermittent pneumatic compression garments are used
on both legs post-operatively when the patient is not ambulating. Before discharge, the patient is tted for 30–40mmHg ankle gradient below-knee compression stockings
and instructed to wear the stockings from waking in the
morning until bedtime. Randomized trials have demonstrated at least a 50% reduction in post-thrombotic morbidity with the use of 30–40-mmHg ankle gradient compression
stockings.
activity, repeat venous duplex and venous function studies
are performed to evaluate ultrasonic patency and vein valve
function, which serve as a baseline for future studies.
18,19
When the patient is fully recovered and back to baseline
References 261
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Guidelines 3.4.0 of the American Venous Forum on catheter-directed thrombolysis and venous thrombectomy for acute
deep vein thrombosis
Grade of evidence
(A:high quality;
B:moderate quality;
C:low or very low quality)
No. Guideline
3.4.1 In patients with symptomatic deep venous thrombosis and
Grade of
recommendation
(1: strong;
2:weak)
1 B
large thrombus burden, particularly in iliofemoral deep
venous thrombosis, we recommend a treatment strategy
that includes thrombus removal.
3.4.2 In patients with symptomatic iliofemoral deep venous
1 B
thrombosis with symptoms of <14 days’ duration, we
recommend catheter-directed thrombolysis if appropriate
expertise and resources are available to reduce acute
symptoms and post-thrombotic morbidity.
3.4.3 We suggest pharmacomechanical thrombolysis, with
2 B
thrombus fragmentation and aspiration, over catheterdirected thrombolysis alone in the treatment of
iliofemoral deep venous thrombosis to shorten treatment
time, if appropriate expertise and resources are available.
3.4.4 In patients with acute deep venous thrombosis, systemic
2 B
thrombolysis is not suggested.
3.4.5 For patients with symptomatic iliofemoral deep venous
1 B
thrombosis who are not candidates for catheter-directed
thrombolysis, we recommend surgical thrombectomy.
Note: Guideline recommendations and suggestions are included in this table. All evidence to the date of the writing of this chapter is con-
sidered; therefore, the strength of these recommendations may differ from previously published guidelines.
the results of the ATTRACT trial will have a major impact on future guidelines.
2,14,15,41
We are certain that
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https://t.me/med1917
Endovascular and surgical management of
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acute pulmonary embolism
ERIN S. DEMARTINO AND RANDALL R. DEMARTINO
21
21.1 Introduction 265
21.2 Pathophysiology of acute PE 265
21.3 Indications for intervention 266
21.4 Fragmentation and suction thrombectomy 266
21.1 INTRODUCTION
Venous thromboembolic events (VTEs) are clinically
important causes of morbidity and mortality, occurring
in 0.8–1 per 1000 person-years. is results in >250,000
admissions for a VTE annually in the United States. A third
of these admissions will be for pulmonary embolism (PE)
at a rate of approximately 0.45 per 1000 person-years.
morbidity of acute pulmonary PE is signicant, and this
diagnosis confers a 15% 28-day mortality rate.1 To direct
treatment, PE is classied by prognostic clinical factors
(Table 21.1), with stratication into massive and submassive
categories on the basis of hemodynamics. For all groups,
the initial treatment for any PE is immediate anticoagulation with unfractionated heparin or, preferentially, with
low-molecular-weight heparin.3 Treatment of low-risk PE
remains anticoagulation therapy alone.4 Patients with massive PE are preferentially treated with thrombolysis, if not
contraindicated.4 However, there is debate regarding the
optimal modality of thrombolytic delivery: by peripheral
systemic or by catheter-directed approaches. Finally, the
preferred approach for the treatment of submassive PE with
thrombolysis and/or the application of catheter-based treatment (CBT) remains intensely debated. e goal of this discussion is to review the interventional approaches for acute
PE for use in clinical practice in massive and submassive PE.
1,2
e
21.2 PATHOPHYSIOLOGY OF ACUTE PE
e hemodynamic response to acute PE will vary for each
patient based on several factors. In addition to the magnitude of the thromboembolic load, humoral factors, including serotonin, thrombin, and histamine release, contribute
21.5 Mechanical thrombectomy devices 267
21.6 Catheter-directed thrombolysis 269
21.7 Surgical pulmonary embolectomy 272
References 274
to the potential for hemodynamic embarrassment. e
patient’s cardiopulmonary reserve also plays a large role
in the tolerance of an acute embolic event. us, a smaller
PE may result in cardiovascular collapse in a patient with
existing cardiopulmonary disease. Conversely, large
thrombus burdens may be tolerated in healthy individuals.
erefore, a patient-specic approach based on the acute
PE stratication (Table 21.1) is needed to guide appropri-
ate treatment.
Acute PE results in increased pulmonary vascular resistance due to two factors. Physical obstruction of the pulmonary vessels increases pulmonary artery (PA) pressures
proportional to the thrombus load. Additionally, the pulmonary vascular bed vasoconstricts in response to hypoxemia. e combination of these two factors results in a
high-pressure circuit. PA pressures are known to increase
when 25%–30% of the pulmonary vasculature is occluded
by thrombus.
classied as severe pulmonary hypertension. In a previously
healthy individual, 40 mmHg may represent the maximum
pressure that the right ventricle (RV) can generate. However,
pre-existing RV hypertrophy may allow the RV to overcome
higher PA pressure.
e obstruction of blood ow through the pulmonary arteries results in increased dead space ventilation.
However, compensatory hyperventilation usually compensates to remove CO2 and can also increase PaO2. However,
mismatch between ventilation and perfusion, intracardiac or intrapulmonary shunting of mixed venous blood,
and alveolar hypoventilation may result in hypoxemia in
patients suering from PE.
Increased RV aerload generated by the extent of thrombus and hypoxemic vasoconstriction can cause signicant
5
5,6
Mean PA pressures of 30–40 mmHg are
6
6
265
266 Endovascular and surgical management of acute pulmonary embolism
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Table 21.1 Classification of acute pulmonary embolism
Risk Definition
Massive Sustained hypotension for >15 minutes or inotropic support due to the PE
Pulselessness
Persistent profound bradycardia (<40 bpm) with evidence of shock
Submassive No systemic hypotension, but either RV dysfunction or myocardial necrosis
RV dysfunction: RV dilation (four-chamber RV diameter/LV diameter >0.9 by US or CT)
Elevated BNP (>90 pg/mL)
Elevated N-terminal proBNP (>500 pg/mL)
ECG changes
Myocardial necrosis: Elevated troponin I (>0.4 ng/mL)
Elevated troponin T (>01 ng/mL)
Low risk No clinical markers for adverse prognosis used to define massive or submassive
Source: Adapted from Jaff MR, McMurtry MS, Archer SL. Circulation 2011;16(123):1788–830.
Note: PE: Pulmonary embolism; bpm: beats per minute; RV: right ventricle; LV: left ventricle; US: ultrasound; CT: computed
tomography; BNP: brain natriuretic peptide; ECG: electrocardiogram.
RV strain. is results in RV dilation, hypokinesis, tricuspid regurgitation, myocardial ischemia, and ultimately
right heart failure. Right ventricular dilation also leads to
intraventricular septal attening, which can impair le
ventricular (LV) function. ese factors can then result in
systemic hypotension from reduced LV preload and overall
LV function, compounding myocardial ischemia. is process occurs over time, such that hemodynamic collapse may
actually occur aer 12–48 hours of relative “normotension”
and hemodynamic stability.
5,7
21.3 INDICATIONS FOR INTERVENTION
Given the pathological milieu of acute PE, treatment needs
to address: (1) prevention of new thrombus formation; (2)
clearance of the obstructing thrombus from the PA (either
rapidly or over time); and (3) reducing RV dysfunction when
present. Current guidelines recommend thrombolysis for
patients with low bleeding risk who have massive PE. In
addition, patients with submassive PE who are thought to be
at risk for adverse prognosis (new hemodynamic instability,
worsening respiratory insuciency, severe RV dysfunction,
or major myocardial necrosis) may be considered for thrombolysis (Figure 21.1).
traindication to systemic thrombolysis (recent intracranial
hemorrhage or surgery, recent spinal surgery, recent head
trauma, intracranial neoplasm, uncontrolled hypertension,
or active or recent bleeding). In addition, systemic thrombolysis carries a 20% risk of bleeding and a 3%–5% risk of
hemorrhagic stroke.8 Moreover, there may be insucient
time to allow for infusion and the eect of systemic thrombolytics in the acute setting. Finally, some patients will fail to
improve despite thrombolytic treatment. In these instances,
alternative treatments for expediting thrombus removal and/
or reducing thrombolytic dosage, such as CBT or surgical
embolectomy, remain important treatment considerations.
3,4
However, some patients have a con-
In massive and submassive PE, RV outow obstruction
can cause severe RV strain. erefore, interventional eorts
to remove the obstructing thrombus can potentially reverse
this pathological state faster than systemic thrombolytic
infusion. Percutaneous CBTs and open embolectomy can
debulk the oending thrombus, expedite thrombolysis,
improve lung perfusion, and/or improve right heart strain
over heparin therapy alone, if systemic thrombolytics are
not possible. Some CBTs may use low-dose or zero thrombolytics to minimize bleeding risk. Although CBTs are appealing for expedited care, they currently remain second-line
therapies to systemic thrombolysis as the initial treatment.
No additional benet of CBTs has been proven over systemic
thrombolysis. However, they remain recommended over
no intervention (i.e., systemic thrombolysis) in conjunction
with anticoagulation for massive and submassive PE.
3
Due to the multitude of approaches for the treatment of
PE, the concept of a PE response team has emerged as a multidisciplinary coordinated eort to streamline and improve
the evolving and complex care of acute PE.9 is multidisciplinary approach may lead to broader national eorts at
improving processes and outcomes for PE.
21.4 FRAGMENTATION AND SUCTION
THROMBECTOMY
e most widely used simple technique is the use of rational
pigtail fragmentation (Figure 21.2). is technique requires
femoral or jugular venous access. A guidewire is passed into
the pulmonary vasculature through the thrombus. In comparison to a traditional pigtail catheter, for fragmentation
of acute PE, the catheter has an oval side hole on its outer
curvature. is allows the catheter to be advanced over the
wire and the wire is used as an axis around which to rotate
(Figure 21.2b). An 8-mm catheter may be useful for segmen-
tal branches and a 12-mm catheter for the main right and
Pulmonary embolism
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Initiate therapeutic
anticoagulation
21.5 Mechanical thrombectomy devices 267
Hypotension?
[SBP<90 mmHg for 15 min]
No
Submassive PE
with RV strain
[abnormal echo or
biomarkers]
Yes
High risk features?
No
No
High risk features with
potential benefit with
thrombolysis
1. Evidence of shock or
respiratory failure
2. Evidence of moderate
to severe RV strain
Low risk PE
Heparin anticoagulation
Contraindication to
No
Initiate systemic
thrombolysis
[or consider catheter
directed thrombolysis]
Massive PE
Yes
Consider multidisciplinary
assessment
thrombolysis?
Yes
Yes
Continue anticoagulation
consider:
• Low dose thrombolytic
• Catheter-based therapy
• Surgical embolectomy
Figure 21.1 Treatment algorithm for pulmonary embolism. PE: pulmonary embolism; SBP: systolic blood pressure.
le pulmonary arteries.
8,10
is procedure can be performed
in less than 30 minutes, resulting in rapid fragmentation
of the thrombus. is technique embolizes the thrombus
distally into smaller branches to restore partial perfusion
of large vessels, improving pulmonary hemodynamics
(Figure 21.2c). Additionally, this intervention increases the
surface area of the thrombus for brinolytic activity. In a
review of interventional techniques, pulmonary fragmentation appears to be clinically eective 80% of the time,
with few complications.11 Finally, additional fragmentation
can be accomplished by deploying an angioplasty balloon
(9–14 mm) into the thrombus.12 e balloon must be undersized compared to the vessel in which it is used to avoid
complications.
8
In addition to fragmentation, it may be possible to
remove the thrombus by aspiration from smaller vessels.
is can be accomplished with any end-hole guide catheter (8 or 9 Fr) placed into the thrombus with the application of negative pressure by means of a syringe. In a
review of CDT treatments, suction thrombectomy, with
or without fragmentation, was technically successful in
40%–100% of cases.
11
21.5 MECHANICAL THROMBECTOMY
DEVICES
e most well-known catheter thrombectomy device is
the AngioJet system (Boston Scientic, Marborough, MA).
e AngioJet is a rheolytic mechanical thrombectomy
device based on Bernoulli’s principle. It creates a lowpressure zone (up to −600 mmHg) in a region of high jet
velocity. e thrombus is fragmented and brought back
into the catheter for removal. is can be combined with
tissue plasminogen activator (tPA) infusion for a pharmacomechanical thrombectomy, whereby tPA is laced
into the thrombus (using either 10 or 20 mg tPA and the
appropriate AngioJet pulse spray-enabled catheter). en,
saline is used for standard rheolytic thrombectomy. e
device has several catheter sizes for peripheral and coronary use. Most catheters are 6 Fr compatible or less (4 Fr
268 Endovascular and surgical management of acute pulmonary embolism
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(b)
Thrombus
Pigtail catheter rotated
around guidewire breaks
up thrombus
Thrombus fragments travel
more distally into lung and
become lodged in smaller
vessels
(a)
(c)
Figure 21.2 Pigtail fragmentation for pulmonary embolism. (a) Large pulmonary embolism in the main left pulmonary
artery obstructing flow. (b) Pigtail catheter is rotated around the wire axis to fragment the thrombus causing distal embolization but restoring flow through the main pulmonary artery. (c) Flow restored with small distal embolization of thrombus.
for coronary use) and require the AngioJet pump tower to
function. is device does not currently have a Food and
Drug Administration (FDA) indication for PE. In spite of
its successful use in the periphery and the initial enthusiasm from good technical success in the treatment of PE,
13,14
signicant complications have been encountered when it is
used in the pulmonary circulation. A systematic review of
all catheter-directed therapies for PE demonstrated that use
of the AngioJet for PE resulted in 76% of all reported complications, even though it was only used in 11% of cases.
Figure 21.3 AngioVac cannula.
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Major and minor complications occurred in 40% and 28%
of patients, respectively. ese complications included bradycardia, heart block, asystole, deep coughing, renal insufciency, hemoglobinuria, and hemoptysis, as well as ve
procedure-related deaths.
8,11,15
Although the cause of these
complications is unknown, possible hypotheses include
the release of adenosine and potassium from hemolysis, or
activation of stretch receptors by the jets. e device now
carries a black box warning about risks of adverse events
and death when used for PE. us, it should not be used in
this setting, since other options with lower risk are readily
available (e.g., fragmentation).
Other thrombectomy devices have been used for the
treatment of PE. e Helix Clot Buster was approved for use
in thrombosed dialysis access, and had been used o-label
for PE. However, the device is no longer available in the
United States. Additionally, e Aspirex catheter (Straub
Medical, Wangs, Switzerland) is a newer device with potential for application in PE, although it is not available in the
United States currently (it carries a venous indication internationally). is device has a high-speed rotating spiral in
the body of the catheter that creates negative pressure. It
allows maceration and aspiration of the thrombus. It has
been shown to be eective during in vitro and in vivo testing16 and in initial clinical reports for PE.17 Additionally, the
Indigo system (Penumbra, Inc., Alameda, CA) has developed a large directional catheter for suction thrombectomy,
however limited data on its use is available to date.
Finally, the AngioVac device (Angiodynamics, Latham,
NY) is a promising emerging catheter-based modality for
the treatment of PE. Based on the instructions for use, the
AngioVac (Figure 21.3) is a venous drainage cannula for
extracorporeal by pass (up to 6 hours). It carries a n additional
indication for the removal of unwanted intravascular material (so thrombus or embolus). It is a 22-Fr coil-reinforced
cannula with a funneled balloon-actuated tip to direct the
thrombus into the cannula (Figure 21.4). It is attached to a
specially designed lter that can be connected to any venovenous bypass centrifugal pump. A second venous access is
necessary for venous return to complete the circuit, as the
device can drain up to 5 L per minute (Figure 21.4). e
device is advanced through a 24-Fr Dryseal sheath (W.L.
Gore, Flagsta, AZ) from the jugular or femoral approach to
enter the pulmonary vasculature. Single reports attest to the
18
feasibility of this device for acute PE.
e only published
institutional series of 14 patients treated with AngioVac
by Donaldson et al. included ve patients treated for PE.
21.6 Catheter-directed thrombolysis 269
However, placement of the catheter in the PA was only performed in three patients.19 Only one of these three patients
had complete evacuation of the mass, and two of the ve
PE cases had adjunctive catheter-directed thrombolysis
performed. Acute drops in hematocrit were common in this
series (11/14), as was need for transfusion (ve patients) and
access site hematomas (two patients).
e authors’ institution has used the AngioVac for PE
cases where thrombolytic treatment is contraindicated and
treatment is warranted (massive or submassive PE with
risk for deterioration). In our limited experience, a jugular
approach is preferred and can be accessed percutaneously.
e use of a sti, pre-curved wire (such as a manually curved
Amplatz wire [Boston Scientic, Natick, MA]) is necessary
to direct the device from the RV into the PA (Figure 21.5).
Extreme care must be taken as RV rupture has been reported
with this technique. Treatment is limited to the rst 2 cm of
the main right and le pulmonary arteries, although theoretically further distal thrombus may be able to be extracted
due to the drainage force of the device. Additionally, due
to the RV outow obstruction created by the device, the
patient should be placed on temporary peripheral extracorporeal membrane oxygenation (ECMO) for safety. is
can be weaned immediately aer the procedure, before
case completion. For simplicity, the AngioVac drainage can
be linked to the ECMO circuit (Figure 21.6). Overall, this
device presents a promising modality for quickly removing
thrombus from the PA without the need for thrombolysis.
However, large doses of heparin are needed for the venovenous bypass circuit to obtain an activated clotting time
(ACT) > 350 seconds. Additionally, there is a risk of dilu-
tional anemia from the uid the circuit adds to the patient’s
intravascular volume. Finally, coordination with cardiac
surgery is a prerequisite, due to the risks of injury to the
heart or pulmonary vessels and the need forECMO.
21.6 CATHETER-DIRECTED
THROMBOLYSIS
In an attempt to reduce the need for large systemic tPA infusions (typically 50–100 mg over 1–2 hours) in the treatment
of PE, the delivery of local thrombolytic agents has been
proposed as a potentially safer option, and can be used as a
standalone treatment or as an adjunct in nearly two-thirds
of all reported CDTs for massive and submassive PE.
is performed aer femoral or jugular access and catheterization of the pulmonary vasculature. A multi-holed lytic
catheter (UniFuse [Angiodynamics, Lytham, NY]) is then
placed within the thrombus, and a thrombolytic agent (urokinase or, more commonly, tPA) is infused unilaterally or
bilaterally (Figure 21.7). For tPA, 1–2 mg/hour is typically
delivered for approximately 15 hours, and then a follow-up
pulmonary arteriogram is performed. is can usually be
done with <30 mg of tPA, hence carrying a theoretically
lower risk of bleeding complications. If extended infusions
(>24 hours) are planned, brinogen levels should be monitored. If the brinogen levels fall precipitously (>50%), or
11
is
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